The present study was performed to evaluate the effects of ormosanine against spinal cord injury (SCI) in rats and to examine the possible molecular mechanism of action. SCI was induced using an impactor device, and rats were treated with ormosanine 10, 50 or 100 mg/kg, p.o., for 10 days after induction of SCI. The effect of ormosanine on SCI was determined by estimating neurological functions and cytokines and parameters of oxidative stress level were estimated in SCI rats. Quantitative reverse transcription polymerase chain reaction, Western blotting analysis and histopathological study were performed on spinal tissue of SCI rats. The data suggested that treatment with ormosanine reversed the alterations of neurological function in SCI rats. Moreover, the levels of cytokines, oxidative stress and reactive oxygen species production were reduced in the ormosanine treatment group compared to the SCI group. The levels of calpain and neuronal nitric oxide synthase activity were significantly reduced in the spinal tissue of the ormosanine treatment group compared to the SCI group. Moreover, ormosanine treatment reduced the percentage of viable neurons in the spinal tissue of SCI rats. In conclusion, the results of this study showed that ormosanine treatment had a protective effect against neuronal injury in spinal cord-injured rats by regulating the peroxynitrite/calpain activity.

中文翻译：

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奥莫卡宁可通过阻断过氧亚硝酸盐/钙蛋白酶的活性来改善脊髓损伤大鼠的神经元功能

进行本研究以评估奥莫卡宁对大鼠脊髓损伤（SCI）的作用，并研究可能的分子作用机理。使用撞击器装置诱导SCI，并在诱导SCI后以10、50或100 mg / kg的奥莫卡因口服处理大鼠10天。通过估计神经功能和细胞因子来确定奥莫卡宁对SCI的作用，并估计SCI大鼠的氧化应激水平参数。对脊髓损伤大鼠的脊髓组织进行了定量逆转录聚合酶链反应，蛋白质印迹分析和组织病理学研究。数据表明，用奥莫卡因治疗可以逆转SCI大鼠神经功能的改变。而且，细胞因子的水平 与SCI组相比，奥莫沙宁治疗组的氧化应激和活性氧产生减少。与SCI组相比，奥莫沙宁治疗组的脊髓组织中的钙蛋白酶和神经元一氧化氮合酶活性显着降低。此外，奥莫卡因治疗降低了脊髓损伤大鼠脊髓组织中存活神经元的百分比。总之，这项研究的结果表明，奥莫卡宁治疗可通过调节过氧亚硝酸盐/钙蛋白酶活性来保护脊髓损伤大鼠的神经元损伤。奥莫沙宁治疗降低了脊髓损伤大鼠脊髓组织中存活神经元的百分比。总之，这项研究的结果表明，奥莫卡宁治疗可通过调节过氧亚硝酸盐/钙蛋白酶活性来保护脊髓损伤大鼠的神经元损伤。奥莫沙宁治疗降低了脊髓损伤大鼠脊髓组织中存活神经元的百分比。总之，这项研究的结果表明，奥莫卡宁治疗可通过调节过氧亚硝酸盐/钙蛋白酶活性来保护脊髓损伤大鼠的神经元损伤。